From these merging hypotheses, we have recently reported that insulin, in the absence of androgen, may drive PCa progression in part through upregulation of SREBP and its downstream enzymes responsible for lipid and steroid synthesis in cell models of prostate cancer, resulting in dramatically increased intratumoral steroid production which is sufficient to reactivate the AR to stimulate PSA expression and secretion [136]. The gene discussed is INS; the disease is prostate carcinoma.